Anesthesia Flashcards
(86 cards)
1
Q
3 different types of anesthesia and the body part it covers
A
- general: insensibility to the whole body + LOC (centrally acting drugs)
- regional: administered specific spinal cord/nerve root level (region of body), still conscious
- local: administered directly to the target tissue, still conscious
2
Q
ASA (American Society of Anesthesia) 1-6
A
ASA 1: healthy
ASA 2: mild systemic disease, no functional limits
ASA 3: moderate systemic disease, some functional limits
ASA 4: severe systemic disease, incapacitating
ASA 5: moribund, will not live 24 hrs without immediate surgery
ASA 6: brain dead, suitable for organ harvest
3
Q
3 areas covered by anesthesia and their definitions
A
- analgesia: pain relief without LOC
- hypnosis: loss of physical awareness +/- LOC
- relaxation: decreased muscle tone
4
Q
4 main medication types used in anesthesia and which area they cover
A
- local/regional anesthesia: analgesia (MAIN) + relaxation
- opioids: analgesia (MAIN) + hypnosis
- general anesthesia: hypnosis (MAIN) + relaxation + analgesia (least)
- muscle relaxants: just relaxation
5
Q
why is analgesia still needed in an unconscious patient?
A
because noxious stimuli causes autonomic reflexes like tachycardia and HTN –> might wake up
6
Q
an example of RA/LA
A
lidocaine
7
Q
different types of opioids (divided into strong and weak, short and long acting)
A
strong:
- short-acting (intraoperative): remifentanil, fentanyl
- long acting (intra + postop): morphine, oxycodone
weak: codeine, dihydrocodeine, tramadol
8
Q
what are some of the issues of LA/RA?
A
- CVS: vasodilation
2. cerebral: sympathectomy (sweating, flushing), neurological sequelae
9
Q
what is the mechanism of action of LA/RA?
A
blocks Na+ channels –> hyperpolarization –> decreased AP –> CVS and cerebral effects
10
Q
what is one benefit LA/RA has over GA in term of side effects
A
respiratory depression spared
11
Q
what are the modes of LA/RA administration? In which of these can opioids be added to enhance pain management?
A
- USS guided
- spinal/epidural +/- opioids
- intrathecal +/- opioids
- wound catheters
- nerve plexus catheters
- topical (patches)
12
Q
modes of administration of GA (2). What are some of the differences between the two?
A
- inhalation agents: slower onset/recovery (washout slower), depends on partial pressure gradient and therefore high doses needed (lungs>blood>brain)
- most adults
- dissolves in lipid cell membrane –> direct physical effect on surface receptors
- slow metabolism (what goes in comes out)
- flexible duration (just keep inhaling as needed)
- Intravenous agents: fast onset/recovery
- most children
- quickly distributes into the tissues and dissolves into lipid membrane (depends on perfusion, although highest affinity for lipids doesn’t go to fat due to low perfusion)
- targets Cl - channels –> hyperpolarization
- wait for excretion by body
13
Q
what are the medications used with each mode of GA?
A
- inhalation: halogenated hydrocarbons (desflurane, sevoflurane, isoflurane)
- IV: propofol (MAIN, fast), thiopental sodium (slow), etomidate, ketamine (children)
14
Q
issues with GA (3) and their management
A
- respiratory:
- decreased hypoxic/hypercarbic drive
- decreased residual capacity and tidal volume –> V/Q mismatch –> increased RR
- paralyzed cilia
solution: O2 + ventilation
- CVS:
- direct (negative inotropic effect on heart –> decreased CO, decreased vascular tone –> vasodilation)
- indirect (vaso/venodilation –> decreased SV, CO, and peripheral resistance)
- pressure injury: positioning + gel padding
15
Q
indications for using muscle relaxant (3)
A
- intubation/ventilation
- when accessing body cavity for surgery
- when immobility is required (neuro/microsurgery)
16
Q
issues with muscle relaxant (3)
A
- awareness
- incomplete reversal –> airway obstruction
- apnoea
17
Q
what are the 3 different types of surgery in the context of pre-op assessment and optimization?
A
- elective planned surgery (months): assessment (6-8 weeks before surgery by anesthetists) + optimization (GP)
- urgent surgery (weeks): assessment + little optimization
- emergency surgery: only assessment
18
Q
what extra things must be done intra + post op for emergency surgery patients?
A
intraoperative: beat by beat invasive monitoring
postop: critical care
19
Q
what is rapid sequence induction (RSI) and when is it needed?
A
a way of achieving airway control while minimizing aspiration risks
- used in those with reflux or not NBM (emergency)
20
Q
what are some of the things to look for in anesthetic preop assessment?
A
- comorbidities, exercise/stress tolerance, identify unknown conditions, FH, etc.
- drug history, allergies, previous addiction
- previous surgery, anesthesia complications
- risks: respi/airway issues, spine deformities, obesity, reflux disease/hasn’t fasted
21
Q
cardiac risk index (used with ASA) - 6
A
a point for each, >= 2 means high risk
- high surgical grade
- congestive heart failure
- ischemic heart disease
- cerebrovascular disease
- DM
- renal failure
22
Q
metabolic equivalent score (MET) (8) - measure of exercise tolerance, with MET2-4 = more morbidity and MET5-9 is less
A
can do the following without getting breathless: MET2: walk around the house MET3: light housework MET4: walk 100-200 meters MET5: walk up hill or up the stairs MET6: walk briskly on flat ground MET7: light exercise MET8: run a short distance MET9: strenuous exercise
23
Q
what is cardiopulmonary exercise testing and why is it quickly becoming a GOLD standard for pre-op anesthesia assessment?
A
OBJECTIVE measure of ECG, O2 consumption, bp –> correlates with post-op morbidity
- all the other scores are subjective
24
Q
what are some of the lifestyle risks in pre-op assessment? What are the effects of each of these? (3)
A
- smoking: septic complications and decreased wound healing
- alcohol: septic complications
- obesity: poorer outcomes
25
what is the best pre-op optimization method and why?
exercise (GOLD standard) - increases the anaerobic threshold --> improved outcomes by 15% per met
26
what are some medications that SHOULD be continued despite NIB?
inhalers, antianginals, antiepileptics
27
what are some medications that can be considered stopping before anesthesia?
anticoagulants (warfarin), DM meds
| - if prostatic heart valve or CVS symptoms, the consider bridging therapy (replacing warfarin with LMWH)
28
what are the 5 different stages of administering GA?
0. (preparation)
1. induction
2. maintenance (phase 1)
- monitoring
3. emergence (phase 2)
4. recovery
5. postop care
29
what are some of the crucial things that happen during the preparation before the induction?
- patient consent + identity check
- IV access
- pre-oxygenation
30
what are the medications given during the induction for GA?
analgesia (fentanyl, alfentanil) + hypnotics (propofol, thiopentone, ketamine, benzodiazepine) +/- muscle relaxants (preferably avoid)
31
after induction and before surgery commences, check to make sure these 5 things are in place for monitoring - what do each of these mean?
1. 3 lead ECG - arrhythmia
2. O2 saturation
3. noninvasive bp cuff - (at least every 5 mins) monitor drop in bp from vasodilation (might need vasopressor)
4. end tidal CO2 - airway patency + blood gas
5. airway pressure monitoring - ventilation quality (separate machine)
32
what happens during maintenance?
- anticipation of key surgical moments and constant adjustment
- advocate for the unconscious patient
33
what are the 4 things that anesthetists must document for every surgery?
1. prescription record
2. observation chart
3. ventilation chart
4. fluids chart
34
explain the process of emergence (in the context of patient management)
stopping anesthetics + reversing muscle relaxants if used --> return of spontaneous breathing + airway reflexes --> remove ventilator --> recovery room
- care of delirious patient as needed
35
where does recovery happen? what happens then?
recovery room, by trained staff + anesthetist review --> ward handover once fully recovered
- ABC management until fully conscious
- initial post-op analgesia
- antinemesis (nausea + vomiting)
36
what are the 2 possible outcomes of post op care?
1. go home (with antinemesis for nausea)
| 2. referred to critical care
37
why is pre-oxygenation important?
100% O2 given to patient before anesthesia --> increases the O2:N2 ratio in the residual capacity --> desaturation time extended to 5 mins
38
Guedel's 4 planes of anesthesia
1. analgesia and amnesia - floaty and relaxed state
2. delirium and unconsciousness - wiggle/excitatory movement in children
3. surgical anesthesia - no response to surgical anesthesia
4. apnoea and death - too much
39
indications for intubation (5)
- protection of airway from aspiration
- muscle relaxation needed
- shared airway with the surgeons
- tight CO2 control needed - with ETT
- limited access to the patient (need to reach)
40
airway management (4)
1. triple airway maneuver + anesthetic/pre-oxygenation mask
2. oropharyngeal/guedel's airway
3. laryngeal mask airway (LMA) - like guedel's airway but sitting over the larynx
4. endoracheal tube (ETT) - most definitive management, inflatable balloon in the trachea to prevent aspiration
41
breathing management (3)
1. spontaneous ventilation - patient breathing
2. controlled ventilation - anesthetist controlled
3. mixed
42
risks of anesthesia (8) - which of these is the most common?
(hypothermia most common)
- anaphylaxis
- induction risks: regurgitation/aspiration, airway obstruction, laryngospasm, hypoxia, CVS instability, cardiac arrest
- awareness (1:13500-1:8200)
- eye injury (1:1000) -
- hypothermia (1:25-1:2)
- pressure injury (1:5)
- VTE (1:100-1:4)
- nerve injury (1:1000)
43
what are the 3 things that can increase the risk of awareness in anesthesia?
1. use of muscle relaxants
2. C-section (specific types of surgery)
3. light planes of anesthesia
44
what are some of the symptoms of awareness and which IS NOT?
NOT movement (just means that muscle relaxant not working enough)
- HTN
- tachycardia
- sweating
45
what intervention (machine) is used to monitor planes of awareness during anesthesia?
EEG (electroencephalogram) machine
46
what are the causes (2) and interventions of eye injury (3)?
causes: eyes cannot blink
1. cornea dries out --> eye injury
2. no protective mechanism
Interventions:
1. taping the eyes are closed
2. lubricating eye drops
3. padding the eyes in lithotomy position (face down)
47
what are the cause (1) and interventions (2) of hypothermia? What about resulting complications (4)?
cause: vasodilation --> decreased core temperature
interventions:
1. monitor temperature at least every 30 mins
2. bear hugger air blankets (esp for long surgeries)
complications:
1. increased site infection
2. increased post op pain
3. haemorrhage
4. increased transfusion risk
48
cause and interventions (2) of pressure in juries
cause: patient completely relaxed, lying in one place without moving for a long time (over tubes accidentally)
interventions:
1. gel padding
2. positioning
49
risk and prophylaxis (3) of VTE
depends on the type of operation
prophylaxis:
1. increased physical activity before operation
2. TED stockings, flowtron (contracts to promote venous return)
3. chemical prophylaxis (dalteparin - anticoagulant) the night before the operation
50
cause and interventions (2) of nerve injury. what are the 3 commonest nerves involved?
```
cause: nerve running over bony prominences are compressed during surgery
Top 3:
1. ulnar n.
2. common fibular n.
3. brachial plexus
interventions:
1. gel padding
2. positioning
```
51
which peripheral nerve fibers do the nociceptive signals travel through? What can be said about the diameter of these fibers?
Ad/C fibers (small)
| (rubbing and non-nociceptive signals through Aa/Ab fibers) - large
52
where in the brain is pain perceived?
cortex - signals from the cortex to thalamus can enhance pain experience by producing expectation of pain
53
which type of drug is tramadol
SNRI (serotonin and noradrenaline reuptake inhibitor)
54
explain the Gate control theory of pain modulation
once it has entered the spinal cord, small nociceptive Ad/C fibers will inhibit the inhibitory interneurons --> signal transmission to the brain, while large nonnocicpetive Aa/Ab fibers will activate the inhibitory interneurons and therefore block the ascending pathway. Therefore with repetitive 'distraction', nonnociceptive signals will > nociceptive signals, and nociceptive pain can be dampened.
55
explain the differences between the characteristic (3) and physiology (2) of nociceptive and neuropathic pain.
nociceptive pain:
- characteristic:
1. inflammatory/physiological - a real tissue injury
2. protective function
3. sharp/dull pain, well localized
- physiology:
1. normal pain signals from injured tissue
2. conventional pain meds effective
neuropathic pain:
- characteristic:
1. caused by NS damage, no real tissue injury
2. no protective function
3. shooting, burning, numbness, pins & needles, NOT well localized
- physiology:
1. abnormal processing of pain signals either from nerve injury (DM, trauma) or dysfunction (fibromyalgia)
2. conventional pain meds ineffective
56
describe the pathology of neuropathic pain (4)
1. increased receptor number --> prolonged pain experience
2. exaggerated firing of nerves
3. abnormal chemicals at the dorsal horn
4. lack of normal inhibitory modulations
57
which type of analgesics are effective in nociceptive pain? (2)
1. simple analgesics (paracetemol, NSAIDs)
| 2. opioids
58
which type of drugs are effective in neuropathic pain? (4)
1. antidepressants (amitriptyline)
2. anticonvulsants (gabapentin, carbamazepine, sodium valproate) - reduces exaggerated firing
3. LA/RA
4. topical agent - capsaicin
59
treatment of neuropathy at different levels of the nervous system: periphery (3), spinal cord (4), brain (2)
periphery:
1. non-pharma: ice, rest, elevation
2. LA/RA
3. NSAIDs (reduce inflammatory soup)
spinal cord:
1. nonpharma: message, acupuncture, transcutaneous electrical nerve stimulation (TENS)
2. LA/RA
3. opioids
4. ketamine (descending pathway pain modulation)
brain:
1. nonpharma: counseling, positive association, hypnosis
2. pharma: paracetemol, clonidine, opioids, amitriptyline
60
treatment of neuropathy at different levels of the nervous system: periphery (3), spinal cord (3), brain (5)
periphery:
1. non-pharma: ice, rest, elevation
2. NSAIDs: decreases prostaglandin and inflammatory soup
3. LA/RA: decreases nociceptive stimulus
spinal cord:
1. non-pharma (message, physio, TENS - uses Gate theory modulation)
2. LA/RA + opiates: epidural/spinal, intrathecal
3. ketamine
brain:
1. non-pharma: psychological help (coping, positive associations, hypnosis)
2. antidepressants
3. paracetemol
4. opioids
5. clonidine (antihypertensive drug, treats hyper reactivity disorder)
61
which analgesic has a synergistic effect with paracetemol?
NSAIDs
62
side effect of paracetemol (1)
1. liver damage
63
side effect of NSAIDs (3)
1. GI bleed
2. renal damage (from decreased blood flow to kidneys, avoid in renal failure)
3. bronchospasm (in asthmatics with previous reaction)
64
side effect of opioids (3)
1. constipation
2. nausea
3. respiratory depression (only strong opioids)
65
side effects of antidepressants (2)
1. anticholinergic effects (urinary retention, glaucoma)
| 2. cognitive decline and dementia associated with long term use
66
describe the WHO pain ladder (mild, moderate, severe) - how to escalate and deescalate
mild: non opioids (paracetemol, NSAIDs)
moderate: weak opioids (codeine)
severe: strong opioids (morphine)
escalation - non-opioids kept at all times, stope step 2 before going to step 3
deescalation - keep non opiods until last
- stop NSAIDs before paracetemol, worse side effects
67
3 different levels of critical care
Level 1: ward-based management
Level 2: high dependency unit, single organ failure
Level 3: intensive care unit, multiple organ failure
68
management of type 1 respiratory failure (2) - also give the different types of ward-based management
1. high flow therapy (HFT) - 70 L/min, routinely used
2. ward-based management - 0-15 L/min O2
- nasal cannula (0-4 L/min), 25-30% O2
- face mask (4-10 L/min), 40% O2 - connected to reservoir bag
- non rebreather mask/trauma mask (15 L/min), 90% O2 - high conc only for rapid increase in O2 sat and not for long term use, connected to reservoir bag
69
why can large volumes of oxygen be given in HFT and not ward-based management?
HFT is connected to heater+humidifier which allows large volume to be given while the ward-based management is connected to the rotameter in the wall and no heater or humidifier
70
what is the purpose of using a lot of volume in HFT (2)?
1. maintains airway in respiratory failure
| 2. high flow rate and therefore patient will get desired O2 sat no matter how badly they are breathing
71
management of type 2 respiratory failure (1) - describe how this works
noninvasive ventilation (NIV) - this will provide both O2 + pressure needed to retain a patent airway and alveoli --> less work for the patient
72
management of severe respiratory failure (1) - describe the 2 mechanisms in which this works
ETT intubation - 1. protects airway from aspiration/reflux, 2. seal air pressure in the lungs and keep airways patent
73
what is usually recommended in prolonged ETT intubation to make things more comfortable for the patient?
tracheostomy - making a hole through the neck in the trachea for NG tube to pass through, bypassing the oropharynx which would allow the patient to swallow and mouth words, both of which would not be possible with the ETT in place.
74
# define the 5 types of shock - which of these are considered disruptive shock (definition + symptoms)?
which of these is the commonest type of shock?
disruptive shock: decreased vessel tone --> low bp and disrupted fluid (flushing, low bp, LOC) - septic, neurogenic, anaphylactic shock
1. septic shock (MAIN): disruptive shock caused by infection, usually bp still low even after fluids
- vessels dilated, heart/volume OK
2. hypovolemic shock: low bp secondary to dehydration/haemorrhage
- low volume, vessels/heart OK
3. anaphylactic shock: disruptive shock caused by severe allergic reaction --> immune response causing vasodilation , also associated with pump failure
- heart/vessels not OK, volume OK
4. neurogenic shock: disruptive shock caused by neural injury (SNS) --> vasodilation
- vessels dilated, heart/volume OK
5. cardiogenic shock: shock caused by damage to the heart (cardiomyopathy, bradycardia, arrhythmia)
- heart not OK, volume/vessels OK
75
why is there no accurate assessment of CO, and what can we do to monitor CO?
CO = HR x SV (there is no accurate measure of stroke volume)
- machines only provide rough estimate of CO and thus must rely on clinical signs such as bp, HR, hydration, temperature, perfusion, hyperdynamics
76
management of cardiovascular failure (4)
1. arterial line
2. central line
3. fluid
4. pharmacology
77
what are some of the differences between arterial and central line - pros and cons of each?
```
arterial line (peripheral arterial 25G cannula) - radial aa (MAIN), brachial aa, femoral aa
- pros: beat by beat monitoring (useful in arrhythmia), can take multiple blood sampling directly, short and therefore fast distribution
- cons: potent drugs that noradrenaline cannot be injected into periphery directly
venous (usually central 6G venous cannula) - IJV (MAIN), subclavian v, femoral v.
- pros: can take multiple sampling directly, central venous blood monitoring, directly injects into central circulation which is safer than peripherally, multiple lines and therefore multiple meds infusion possible, aseptic
- cons: long and thin and therefore slower distribution
```
78
what are some of the pharmacological management of CVS failure? Divide these into vasopressors (2) and inotropes (2) and describe the function of each
1. vasopressors (increased preload + bp)
- metaraminol (MAIN a1 agonist, vasoconstriction + b activity, increased contractility)
- noradrenaline (MAIN a1 agonist, vasoconstriction + b activity, increased contractility) - MUCH more potent and thus only centrally given
2. inotropes (increased contractility --> increased CO)
- adrenaline (MAIN b activity, increased contractility + a1 agonist, vasoconstriction) - use in shock if first line doesn't work
- dobutamine (PURE b activity, contractility)
79
How is fluid given in CVS failure? Describe in terms of type (2), goal (2), and maximum limit of fluid management
type:
1. colloid - large osmotically active molecules, stay in vascular tree and useful in resus
2. crystalloid - small molecules (0.9% saline, dextrose), quick distribution into tissues, but still useful for resus
goals:
1. maintenance: keeping patient hydrated during NBM
2. resuscitation: patient intravascularly depleted, and rehydartion is needed to restore haemodynamics (bp, HR)
maximum limit: 30 mL/kg, max 250-500 mL
- stick to lower limit 250 if high risk of fluid overload like chronic HF
80
4 types of neurological failure - which of these is the main one?
1. metabolic (MAIN) - disease process resulting in ACUTE systemic upset and decreased consciousness (sepsis, inflammation, metabolic upset (renal failure, uremia, electrolyte imbalances))
2. trauma - injury to the head --> brain swelling --> coning, decreased consciousness or death
3. infection - decreased consciousness due to infection (meningitis, encephalitis, secondary metabolic upset from infection)
4. stroke - vascular disturbance in the brain --> decreased consciousness
81
what is the main complication of neurological failure and what are some of the interventions (3)?
complication: decreased consciousness level --> failure of airways + respiratory functions
interventions:
1. ventilation
2. fluid management
3. involve critical care in worse case scenario (patient unlikely to return to normal function after this)
82
should the arterial line or central line be picked in a patient with hypovolemic shock and why?
arterial line should be picked although there is risk of tissue damage because it is much quicker and the patient urgently needs resus.
83
which CVS failure meds are used in which kinds of shock and why?
1. vasopressors (increased preload through venoconstriction, increased bp through vasoconstriction) - septic shock
2. inotropes (increased heart contractility --> increased CO) - cardiogenic shock
84
what the 2 of the markers for haemodynamics, and which of these is the main one?
1. urine output (MAIN)
| 2. HR, bp
85
what should the next step be if there is no improvement in shock even when max fluid is used? (2)
1. give CVS failure mediations
| 2. involve critical care
86
can patient with trauma neurological failure attend surgery right away? If not, what interventions must be done first? (2)
No, they must first be stabilized by anesthetists:
1. ventilation --> increasing O2 to brain + removing CO2 will decrease the swelling
2. fluid management --> increased perfusion to the brain (careful of overload)
